Spinal Cord Dysfunction
Neurology Rotation Lecture Series
Last Updated by Lindsay Pagano
Summer 2013
Case Presentation
The ED consults you on a 15 year old female with LE numbness and
weakness.
• Previously healthy
• Symptoms began 4 days go with back pain
• Subsequent development of numbness and weakness of both legs
• Has lost control of urination and defecation
• General exam: + for palpable suprapubic mass
• Neuro Exam: normal except for
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LE 0/5 throughout and symmetrically with hypotonia
Below the umbilicus, there is complete loss of light touch, temperature and pinprick
BLE with impaired vibration sense
Poor rectal tone
DTRs absent in BLE, toes mute
• Differential?
Composition of the Spinal Cord
Localizing Spinal Cord Lesions
Upper Motor Neuron
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aka supranuclear, neuron is in CNS
weakness
spastic, increased tone
increased DTRs (muscle spindle threshold
decreased)
clonus: contraction of one group mm 
initiate monotactic reflexes in their
antagonists
some atrophy- disuse
toes up
no fasciculations
Lower Motor Neuron
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aka infranuclear, nuclear; CNS neuron or
PNS fibers
WEAKNESS
flaccid, decreased tone
decreased DTRs (efferent limb
interrupted)
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no clonus
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ATROPHY
toes down
fasciculations present (exotoxicity)
Localizing the Lesion, continued
• History
– Onset of symptoms
– Incontinence
– Sexual dysfunction (depending on age)
• Exam
– Motor
• tone
• strength
– Reflexes
• DTRs
• clonus
– Sensory
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pain and temperature
vibration, joint position sense
sensory level on the trunk
further dermatomes on the extremities
Spinal Cord Lesions
• Acutely: Spinal Shock
– Initial injury with flaccid paralysis and mute reflexes, including plantar
– Gradual recovery and development of UMN, LMN signs
– Upgoing toes first to develop
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Transverse myelitis: relate to level of lesion; gradual onset; MRI with contrast
MS: related to level of lesion; gradual onset; MRI with contrast
Mass: eg tumor, abscess: related to level of lesion; gradual onset; MRI with contrast
Stroke: typically anterior cord; MRI with diffusion and ADC map
– Pain in a band around the abdomen
– Symptoms related to level of lesion; sudden onset
• Brown-Séquard Syndrome: cord hemisection
– IL: weakness, loss of fine touch, vibration, proprioception distal to the lesion
– CL: loss of pain and temperature 1-2 levels below the lesion
• Atlantoaxial instability: C1-2 articulation
– Down syndrome: transverse ligament instability; 10-30% of Down syn patients
– Subluxation symptoms are those of cord dysfunction at those levels
PREP question
During the health supervision visit for a 6 week old boy, his father
expresses concern that his son “doesn’t look like” his other children. Growth
parameters are normal except for a head circumference of 35.5 cm (<5th
percentile).
On PE, you note that the infant does not appear to fixate or track
your face visually. There is a “slip through” on vertical suspension and
“draping over” on horizontal suspension. DTRs are brisk. Moro reflex is
present and brisk.
Of the following, the MOST likely cause of this infants hypotonia is:
A. Anterior horn cell disease
B. Congenital brain malformation
C. Congenital myasthenic syndrome
D. Congenital myopathy
E. Spinal cord disease
B. Congenital brain malformation
• Hypotonia
– Localize! UMN versus LMN signs, axial vs appendicular
– Take into account growth parameters, especially HC, as well as features
such as tracking
• Regarding the other choices:
A. Anterior horn cell disease: wouldn’t cause microcephaly or increased
reflexes
C. Congenital myasthenic syndrome: wouldn’t cause microcephaly or brisk
reflexes
D. Congenital myopathy: no microcephaly or poor visual tracking
E. Spinal cord disease: wouldn’t cause microcephaly or poor visual tracking